Pain is an unpleasant sensory and emotional experience caused by actual or potential tissue damage. It serves a protective function by warning us of damage. Pain is transmitted through specialized pain pathways and is classified based on duration, location, and source. There are different types of pain receptors that detect various painful stimuli and transmit signals through different nerve fiber types to the central nervous system where pain is perceived.

1. Pain and Pain Pathways
Anjali Savita
MDS I
Dept of Conservative Dentistry and
Endodontics

2. “I don’t accept the maxim ‘there is no gain
without pain’, physical or emotional. I believe it
is possible to develop and grow with joy rather
than grief; however when pain comes my way, I
try to get the most growth out of it”
- Alexa Mclaughlin

3. Contents
Introduction
Definition
History
Incidence
Related Terms
Characteristics of pain
Classification of pain
Pain receptors
Pathway of pain sensation
Theories of pain
Pain pathway of
Maxillofacial Region
Dental pain
References

4. Introduction
Pain is the commonest symptom which physician are
called upon to treat.
Pain is an intensely subjective experience, and is
therefore difficult to describe.
 Physiology of pain has taught us a lot about neural
function in general.
It has two universal features. First, its an unpleasant
experience. Second, it is evoked by a stimulus which is
actually or potentially damaging to living tissue.

5. That is why, although it is unpleasant, pain serves a
protective function by making us aware of actual or
impeding damage to the body.
Like all sensory experiences, pain has two
components, the first component is awareness of
painful stimulus and second one is emotional impact(or
effect) evoked by experience.
While the awareness is localized to the area
stimulated, experience involve the whole being.
That is why when a finger is hurt, the whole person
suffers.

6. Definition of Pain
Pain is “an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described
in terms of such damage”.
- International association for the study of Pain.
“An unpleasant emotional experience usually initiated by
noxious stimulus and transmitted over a specialized neural
network to the CNS where it is interpreted such as.”
- Monheim’s textbook of local anaesthesia

7. History
Derived from Latin word “poena” meaning punishment from
God.
Homer thought pain is due to arrows shot by God.
Aristotle who was first to distinguish five physical senses
considered pain to “ the passion of the soul” that somehow
resulted from intensification of other sensory experience.
Plato contented, pain and pleasure arose from within the
body.
Bible makes reference to pain not only in relationship to
injury and illness but also an anguish of the soul.

8. Incidence of Pain
According to Cohen- it was found that 21.8% of adult in the united states
experiences orofacial pain symptoms within 6 months of study.
The most common pain was toothache, which was estimated to have
occurred in 12.3% of the population.
Dental pain is highly prevalent among children, the association being most
apparent in lower socioeconomic groups with reduced access to care.
The prevalence of dental pain was 35% among all pain.
Dental pain has been associated with many factors, such as low
socioeconomic status, high levels of dental caries and restricted access to
dental services.

9. Related Terms
Allodynia
Hyperalgesia and hypoalgesia
Hyperpathia
Causalgia
Neuralgia

10. Characteristic of Pain
Threshold and Intensity
If the intensity of the stimulus is below the threshold(sub
threshold) pain is not felt. As the intensity increases more
and more, pain is felt more and more according to Weber-
Fechner’s Law.
As per this law magnitude of sensation felt is directly
proportional to log of intensity of stimulus

11. Adaptation
 Pain receptors show no adaptation, so the pain continues as
long as receptors are stimulated.
Localization of pain
 Pain sensation is somewhat poorly localized, however
superficial pain is comparatively better localized than deep pain.
Influence of the rate of damage on intensity of pain
 If rate of damage(tissue injury) is high, intensity of pain is also
high.

12. Classification of Pain
Based on source/ location/ referral & duration
Pain
Visceral
Acute / Traumatic
pain
Chronic pain
Malignant pain
/cancer painSomatic Non- malignant
benign pain
Superficial Deep
Musculo-
skeletal
Neuropath
-ic

13. ACUTE PAIN
Acute has a sudden onset, usually subsides quickly and is characterized by sharp,
localized sensations with an identifiable cause.
Lasts > 30 days and occurs after muscle strains and tissue injury such as trauma or
surgery.
A poorly treated pain can cause psychological stress and compromise the immune
system due to the release of endogenous corticosteroids
Acute pain is usually characterized by increased autonomic nervous system activity
resulting in psychological symptoms such as anxiety
 Tachypnoea
 Tachycardia with hypertension
 Pallor
 Diaphoresis
 Pupil dilation

14. VISCERAL PAIN
Visceral pain is a type of nociceptive pain that comes from the
internal organs.
Unlike somatic pain it is harder to pinpoint, described as general
aching or squeezing pain
It is caused by the activation of pain receptors in the chest,
abdomen, or pelvic areas.
In cancer patients pain is caused by tumor infiltration,
constipation, radiation & chemotherapy.

15. SUPERFICIAL PAIN
It is also known as
cutaneous pain.
It arises from superficial
structures such as skin &
subcutaneous tissues.
It is a sharp, bright pain
with a burning quality and
may be abrupt or slow in
onset.
DEEP SOMATIC PAIN
It originates in deep body
structures such as
periosteum, muscles,
tendons, joints & blood
vessels
Strong pressure, ischemia,
tissue damage act as stimuli
for brain damage
Radiation of pain from
original site of injury occur.

16. CHRONIC PAIN
Chronic pain is defined as pain lasting longer than 3 to 6
months.
It begins when pain persists after the initial injury has
healed.
It is persistent or episodic pain of duration or intensity
that adversely affects the function and well being of the
patient.
It may be nociceptive, inflammatory, neuropathic or
functional in origin.

17. It occurs in 60-90 % of patients
with cancer.
Pain can be related to the tumor
or cancer therapy or may be
idiosyncratic.
Pain may also be found at the
metastasized regions and
treatment interventions may
activate peripheral nociceptors.
Pain can be somatic/visceral
CHRONIC NONCANCER PAIN
Pain may last for many years
and is considered progressive in
nature.
May be nociceptive, neuropathic
or mixed in nature.
CHRONIC MALIGNANT PAIN

18. NEUROPTHIC PAIN
 Neuropathic pain is a result of an injury or malfunction of the
nervous system.
It is described as
 Aching
 Throbbing
 Burning
 Shooting
 Tenderness/ sensitivity of skin

19. • Acute hemorrhagic neuralgia
• Diabetes
• HIV
• Chemotherapeutic agents
Peripheral
Pain
•Central stroke pain
•Trigeminal neuralgia
Central
Pain

20. MUSCULOSKELETAL PAIN
This a type of chronic non cancer pain occurring due to
musculoskeletal disorders such as
Rheumatoid arthritis
Osteoarthritis
Fibromyalgia
Peripheral neuropathies

21. BASED ON TRANSMISSION
FAST PAIN
Felt about 0.1 sec after a
painful stimulus is applied.
It is described as sharp pain,
pricking pain, acute & electric
pain
Fast sharp pain is not felt in
most deeper tissues of the
body.
Due to activation of Aδ fibres
SLOW PAIN
 Usually begins after 1 sec or
more and may range from
seconds to minutes.
 Described as slow, burning,
aching, throbbing, nauseous
pain and chronic pain
 Associated with tissue
destruction.
 Due to activation of C fibres

22. OTHER TYPES OF PAIN
REFERRED PAIN
Pain that originate due to
irritation of a visceral organ and
felt not in organ but in some other
somatic structure as well which
has innervated by the same neural
segment.
Usually applies to pain that
originates from the viscera
 E.g. The pain associated with MI
commonly is referred to the left
shoulder arm, neck & chest.
BREAKTHROUGH PAIN
Pain is intermittent, transitory.
Usually lasts from minutes to
hours and can interfere with
functioning.
E.g. Neuropathic pain, Lower
back pain

24. Practical clinical classification of cranio facial pain
General Classification Origin of Pain Quality of Pain
Extra cranial Structure Craniofacial region varies
Referred pain from remote
pathologic sites
Distant organs and
structures
Aching and pressing
Intracranial pathosis Brain and related
structures
Varies
varies
Neurovascular Blood vessels Throbbing, Pulsing,
Pounding

25. General Classification Origin of Pain Quality of Pain
Neuropathic Sensory nervous
system
Shooting, sharp,
burning pain
Causalgic Sympathatic nervous
system
Burning
Muscular Muscles Deep aching, tight

26. OROFACIAL PAIN CLASSIFICATION (OKESON)
AXIS I (physical conditions)
 Somatic pain
Superficial Somatic pain
• Cutaneous pain
• Mucogingival
Deep Somatic Pain
• Muscle pain
• TMJ pain
• Osseous pain
• Periodontal pain
 Visceral pain
• Pulpal pain
• Vascular pain
• Neurovascular pain
• Visceral mucosal pain
• Glandular, ocular, auricular pain

27. AXIS II (psychologic conditions)
 Mood disorders
 Anxiety disorders
 Somatoform disorders
 Other conditions
• Psychologic factors affecting a medical condition

28. Pain Receptors
NOCICEPTORS or PAIN RECEPTORS are sensory receptors that
are activated by noxious insults to peripheral tissues.
The receptive endings of the peripheral pain fibres are free
nerve endings.
These receptive endings are widely distributed in the
 Skin
 Dental pulp
 Periosteum
 Meninges

31.  SILENT
NOCICEPTORS
These receptors
activated at the
time of
inflammation
only.
Upto 40% of C
fibers and 30% of
Aδ fibers are
silent
nociceptors.
UNIMODAL
NOCICEPTOR
S
These
receptors
respond
exclusively to
one modality
i.e. either
noxious
chemical or
heat stimuli.
POLYMODAL
NOCICEPTORS
These receptors
are sensitive to
several varieties
of noxious stimuli
These do not have
a specialized and
simple nerve
endings in the
periphery.

32. NERVE FIBRES INVOLVED IN PAIN TRANSMISSION
A FIBRES
A – BETA
FIBRES
 Large
 Myelinated
 Fast
conducting
 Low
stimulation
threshold
 Respond to
light touch
C FIBRES
Small & unmyelinated
Very slow conducting
Respond to all types
of noxious stimuli
Transmit prolonged
dull pain
Require high intensity
stimuli to trigger a
response
A – DELTA
FIBRES
 Small
 Lightly
Myelinated
 Slow
conducting
 Respond to
heat, pressure,
cooling &
chemicals
 Sharp sensation
of pain

34. NEURO TRANSMITTER S INVOLVED IN PAIN
ACTIVATION OF NOCICEPTORS BY INTERACTING WITH OTHER
CHEMICAL MEDIATORS
PGI2
LTs
SUBSTANCES EXITING NCs
HISTAMINE POTASSIUM
ATP
STIMULATION OF
NOCICEPTORS BRADYKININ
DISCHARGE OF PAIN
RELEASING SUBSTANCES
BY NOCICEPTORS
SUBSTANCE – P
GLUTAMATE
SENSITIZATION OF
NOCICEPTORS
PGE2
PGI2

35. PATHWAYS OF PAIN SENSATION
The pathways of pain sensation are as follows
Pathway from skin & deeper tissues
Pathway from face – pain sensation is carried by trigeminal nerve
Pathway from viscera – pain sensation from thoracic &
abdominal viscera are transmitted by sympathetic nerves & from
oesophagus, trachea & pharynx by glossopharyngeal nerves
Pathway from pelvic region – conveyed by sacral
parasympathetic nerves

36. PATHWAY FROM SKIN & DEEPER TISSUES
FIRST
FIRST ORDER
NEURONS
These are the cells in the posterior nerve root ganglia, receive impulses from pain receptors through dendrites
These impulses are transmitted through the axons to spinal cord
Impulses are transmitted by Aδ fibre or C fibres
SECOND ORDER
NEURONS
The neurons of marginal nucleus & substantia gelatinosa form the II order neurons
Fibres from these neurons ascend in the form of the lateral spinothalamic tract
Fibres of fast pain arise from neurons of the marginal nucleus
The fibres of slow pain arise from neurons of substantia gelatinosa
THIRD ORDER
NEURONS
The neurons of pain pathway are the neurons in Thalamic nucleus, reticular formation, tectum, gray matter
around the aqueduct of sylvius
Axons from these neurons reach the sensory area of cerebral cortex or hypothalamus

37. PAIN PATHWAYS
ASCENDING PAIN PATHWAY

38. DESCENDING INHIBITORY PAIN PATHWAY

39. Pain pathway of Maxillofacial region
5TH cranial nerve or trigeminal nerve is the principle
sensory nerve of head region.
Any stimulation in the area of trigeminal nerve is first
received by both myelinated and unmyelinated fibers,
and conducted as an impulse along afferent fibers of
ophthalmic, maxillary and mandibular branches into
semilunar and gasserian ganglion.
Pain impulse descend from the pons by spinal tract
fibers of trigeminal nerve through the medulla

41. MECHANISMS OF PAIN
Pain sensation involves a series of complex interactions
between peripheral nerves & CNS.
Pain sensation is modulated by excitatory and
inhibitory NTs released in response to stimuli.
Sensation of pain is composed of 4 basic processes
Transduction
Transmission
Modulation
Perception

42. TRANSDUCTION
Activation of nociceptor
 Intense thermal and mechanical stimuli, noxious chemicals,
noxious cold
 Stimulation of inflammatory mediators
Damaged tissue release bradykinin, potassium, histamine,
serotonin and arachidonic acid.
Arachidonic acid produce prostaglandins and leukotrienes.

43. TRANSMISSON
Process by which peripheral nociceptive information is
relayed to CNS.
First order neuron synapses with the secondary order neuron
from where impulse is carried to higher structures of brain.
Repeated or intense C fibre activation brings specific changes
on N-methyl-D-aspartate receptors resulting in central
sensitization, thus, response of second order neurons increases
as well as size of the receptive field also increases.

44. MODULATION
 It is the mechanism by which transmission of impulse to the brain is
either inhibited or excitated.
Endogenous opioid peptides are naturally occurring paindampening
neurotransmitters and neuromodulators employed in suppression and
modulation of pain because they are present in large quantities in areas
of brain associated with these activities.
PERCEPTION
It is the subjective experience of pain. It is the sum of complex activities
in CNS that may shape the character and intensity of pain perceived and
ascribe meaning to pain.

46. PAIN THEORIES
Pain theories are proposed to offer the possible physiologic
mechanisms involved in pain. They are as follows
 Specificity theory
 Pattern theory
 Neuro-matrix theory
 Gate control theory

47. SPECIFICITY THEORY
Proposed by Johannes Muller in 1842.
According to this theory pain is a specific modality
equivalent to vision and hearing.
This theory states pain as separate modality evoked by
specific receptors(free nerve endings) that transmit
information to pain centers or regions in the forebrain
where pain is experienced.

48. PATTERN THEORY
Proposed by Goldscheider in 1894.
According to this theory pain sensation depends on Spatio-
temporal pattern of nerve impulse reaching the brain.
According to Woddell (1962) warmth, cold and pain are words
used to describe reproducible spatio temporal pattern or codes
of neural activity evoked from skin by changes in environment.
The precise pattern of nerve impulse entering the CNS will be
different for different regions, and will vary for person to person
because of normal anatomical variations.

49. NEUROMATRIX THEORY
This theory was put forward by MELZACK
This theory explains the role of brain in pain as well as the multiple
dimensions and determinants of pain.
According to this theory the brain contains a widely distributed neural
network called the body self Neuromatrix that contains somatosensory,
limbic, & Thalamocortical components
The body self Neuromatrix involves multiple input sources such as
 Somatosensory inputs
 Other impulses/ inputs affecting the interpretation of the situation
 Various components of stress regulation systems
 Intrinsic neural inhibitory modulatory circuits

50. GATE CONTROL MECHANISM
Proposed by MELZACK & WALL IN 1965.
According to this theory, the pain stimuli transmitted by
afferent pain fibres are blocked by GATE MECHANISM
located at the posterior gray horn of the spinal cord
If the gate is open pain is felt, and if the gate is closed pain
is suppressed
Impulses in A – δ & C – fibres can be blocked by
modulated by A – β activity that can selectively block
impulses from being transmitted to the transmission cells
in the spinal cord and then to CNS resulting in no pain

51. ROLE OF BRAIN IN GATE CONTROL MECHANISM
Gates in spinal cord are
open
Pain signals reach the
thalamus through lateral
spinothalamic tract
Signals are processed in
thalamus
Signal are sent to sensory
cortex & perception of
pain occurs in cortex
Signals are sent from
cortex back to spinal cord
and the gate is closed by
releasing pain relievers
such as opioid peptides
Minimizing the
severity & extent of
pain

53. Tooth pulp pain
Exposure of dentinal tubules causes toothache &
other non noxious sensation.
Both Aδ & C fibers respond to stimuli in dentine
Transmission of stimuli across dentin, mediated by
movement of fluid in dentinal tubules.
Fibers terminate at medullary dorsal horn &
synapse and also at trigeminal sensory nucleus

54. From trigeminal nucleus send to thalamus & sensory
cortex.
Pulpal innervation are capable of regenerating &
reinnervating

55. Conclusion
Anxiety is determinant for pain during dental care & pain
is related to local anesthetic procedures. There are
evidences that dentists attitude are determinants for pain.

56. References
Essential of oral physiology- Robert M Bradley
Textbook of medical physiology- Guyton & Hall
Essential of medical physiology- K.Sembulingam & Prema Sembulingam.
Textbook of human physiology- S Chand
Determinants of painful experience during dental treatment- Ruth Suzanne et al
Rev.Dor 2012;13(4)
Case report study on Brown sequard syndrome- Ponachi et al Neurology Asia
2007;12;65-67
Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin P.Rae anesthesia
& intensive care medicine; 2010;12(1)